...
机译:IL-33表达的降低会加剧糖尿病小鼠缺血/再灌注所致的心肌损伤
1Division of Cardiology, Department of Medicine, the Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, China 2Critical Illness Research, Lawson Health Research Institute, 800 Commissioners Road E., VRL Rm A6-138, London, ON, Canada N6A 4G5 3Critical Care Western, Department of Medicine, University of Western Ontario, London, Ontario, Canada 4Department of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada N6A 4G5;
机译:IL-33表达的降低会加剧糖尿病小鼠缺血/再灌注引起的心肌损伤
机译:实验性糖尿病通过促进线粒体裂变来加剧缺血/再灌注诱导的心肌损伤:对心肌SIRT1的下调和随后的AKT / DRP1相互作用的作用
机译:唾液酸化刘易斯(X)单克隆抗体在缺血/再灌注大鼠心脏中表达唾液酸化Lewis(X)并减轻心肌再灌注损伤
机译:抑制常规心脏肥大细胞脱粒可能预防缺血性和再灌注诱导的心肌损伤
机译:在2型糖尿病模型中,腔内对损伤的反应被夸大了。
机译:校正:在重复性阻塞的大鼠模型中心血管药物减弱了心肌对缺血性和再灌注性损伤的抵抗力
机译:IL-33表达的减少夸大了患有糖尿病小鼠的缺血/再灌注诱导的心肌损伤